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Kinetics of glyphosate and aminomethylphosphonic acid sorption onto montmorillonite clays in soil and their translocation to genetically modified corn

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Journal of Environmental Sciences 2024年第1期135卷 669-680页

作者： Meichen Wang Kelly J Rivenbark Timothy D Phillips Veterinary physiology and pharmacology College of Veterinary Medicine and Biomedical SciencesTexas A&M UniversityTX 77845USA

The co-occurrence of glyphosate(GLP)and aminomethylphosphonic acid(AMPA)in contaminated water,soil,sediment and plants is a cause for concern due to potential threats to the ecosystem and human health.A major route of exposure is through contact with contaminated soil and consumption of crops containing GLP and AMPA residues.However,clay-based sorption strategies for mixtures of GLP and AMPA in soil,plants and garden produce have been very limited.In this study,in vitro soil and in vivo genetically modified corn models were used to establish the proof of concept that the inclusion of clay sorbents in contaminated soils will reduce the bioavailability of GLP and AMPA in soils and their adverse effects on plant growth.Effects of chemical concentration(1–10 mg/kg),sorbent dose(0.5%-3%in soil and 0.5%-1%in plants)and duration(up to 28 days)on sorption kinetics were studied.The time course results showed a continuous GLP degradation to AMPA.The inclusion of calcium montmorillonite(CM)and acid processed montmorillonite(APM)clays at all doses significantly and consistently reduced the bioavailability of both chemicals from soils to plant roots and leaves in a dose-and time-dependent manner without detectable dissociation.Plants treated with 0.5%and 1%APM inclusion showed the highest growth rate(p≤0.05)and lowest chemical bioavailability with up to 76%reduction in roots and57%reduction in leaves.Results indicated that montmorillonite clays could be added as soil supplements to reduce hazardous mixtures of GLP and AMPA in soils and plants.

关键词： Glyphosate AMPA Adsorption Soil remediation Plant Hydroponic system

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Role of N-formyl peptide receptor 2 in germinal matrix hemorrhage:an intrinsic review of a hematoma resolving pathway

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Neural Regeneration Research 2024年第2期19卷 350-354页

作者： Jerry Flores Jiping Tang Department of physiology&pharmacology Loma Linda University School of MedicineLoma LindaCAUSA

Germinal matrix hemorrhage is one of the leading causes of morbidity,mortality,and acquired infantile hydrocephalus in preterm infants in the United States,with little progress made in its clinical management.Blood clots have been shown to elicit secondary brain injury after germinal matrix hemorrhage,by disrupting normal cerebrospinal fluid circulation and absorption after germinal matrix hemorrhage causing post-hemorrhagic hydrocephalus development.Current evidence suggests that rapid hematoma resolution is necessary to improve neurological outcomes after hemorrhagic stroke.Various articles have demonstrated the beneficial effects of stimulating the polarization of microglia cells into the M2 phenotype,as it has been suggested that they play an essential role in the rapid phagocytosis of the blood clot after hemorrhagic models of stroke.N-formyl peptide receptor 2(FPR2),a G-protein-coupled receptor,has been shown to be neuroprotective after stroke.FPR2 activation has been associated with the upregulation of phagocytic macrophage clearance,yet its mechanism has not been fully explored.Recent literature suggests that FPR2 may play a role in the stimulation of scavenger receptor CD36.Scavenger receptor CD36 plays a vital role in microglia phagocytic blood clot clearance after germinal matrix hemorrhage.FPR2 has been shown to phosphorylate extracellular-signal-regulated kinase 1/2(ERK1/2),which then promotes the transcription of the dual-specificity protein phosphatase 1(DUSP1)gene.In this review,we present an intrinsic outline of the main components involved in FPR2 stimulation and hematoma resolution after germinal matrix hemorrhage.

关键词： AnxA1 FPR2 GMH hematoma resolution hemorrhagic stroke M1 M2 microglia polarization microglia phagocytosis

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Unraveling the potential of acute intermittent hypoxia as a strategy for inducing robust repair in multiple sclerosis

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Neural Regeneration Research 2024年第11期19卷 2339-2340页

作者： Valerie M.K.Verge Nataliya Tokarska Justin M.Naniong Department of Anatomy Physiology and PharmacologyUniversity of SaskatchewanSaskatoonSKCanada Cameco MS Neuroscience Research Center University of SaskatchewanSaskatoonSKCanada

Multiple sclerosis(MS)is a debilitating inflammatory disease of the central nervous system characterized by immune-mediated segmental demyelination and variable degrees of axonal and neuronal degeneration that contribute to disability.Inducing efficient and effective repair programs following demyelination is a major goal and challenge in MS.Conventional MS therapies focus largely on modulating the immune aspects of the disease contributing to lesions.While this alleviates some symptoms and mitigates damage,it does not tackle the fundamental challenge of effective remyelination,which few MS patients experience,especially in the progressive phase of the disease.

关键词： sclerosis degeneration damage

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Adenosine A_(2A)receptor blockade attenuates excitotoxicity in rat striatal medium spiny neurons during an ischemic-like insult

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Neural Regeneration Research 2024年第2期19卷 255-257页

作者： Elisabetta Coppi Federica Cherchi Alasdair J.Gibb Department of Neuroscience PsychologyDrug Research and Child HealthUniversity of FlorenceFlorenceItaly Department of Neuroscience Physiology and PharmacologyUniversity College LondonLondonUK

During brain ischemia,excitotoxicity and peri-infarct depolarization injuries occur and cause cerebral tissue damage.Indeed,anoxic depolarization,consisting of massive neuronal depolarization due to the loss of membrane ion gradients,occurs in vivo or in vitro during an energy failure.The neuromodulator adenosine is released in huge amounts during cerebral ischemia and exerts its effects by activating specific metabotropic receptors,namely:A_(1),A_(2A),A_(2B),and A_(3).The A_(2A)receptor subtype is highly expressed in striatal medium spiny neurons,which are particularly susceptible to ischemic damage.Evidence indicates that the A2Areceptors are upregulated in the rat striatum after stroke and the selective antagonist SCH58261 protects from exaggerated glutamate release within the first 4 hours from the insult and alleviates neurological impairment and histological injury in the following 24 hours.We recently added new knowledge to the mechanisms by which the adenosine A2Areceptor subtype participates in ischemia-induced neuronal death by performing patch-clamp recordings from medium spiny neurons in rat striatal brain slices exposed to oxygen and glucose deprivation.We demonstrated that the selective block of A2Areceptors by SCH58261 significantly reduced ionic imbalance and delayed the anoxic depolarization in medium spiny neurons during oxygen and glucose deprivation and that the mechanism involves voltage-gated K+channel modulation and a presynaptic inhibition of glutamate release by the A2Areceptor antagonist.The present review summarizes the latest findings in the literature about the possibility of developing selective ligands of A2Areceptors as advantageous therapeutic tools that may contribute to counteracting neurodegeneration after brain ischemia.

关键词： adenosine A_(2A)receptors anoxic depolarization brain ischemia glutamate excitotoxicity medium spiny neurons oxygen and glucose deprivation

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Pleiotropic attenuating effect of Ginkgo biloba against isoprenalineinduced myocardial infarction via improving Bcl-2/mTOR/ERK1/2/Na^(+) , K^(+) -ATPase activities

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Chinese Herbal Medicines 2024年第2期16卷 282-292页

作者： Jerome Ndudi Asiwe Abodunrin Adebayo Ojetola Nwoke Enekabokom Ekene Esthinsheen Osirim Anthony Chibuzor Nnamudi Benjamin Oritsemuelebi Jackson Erozueme Onuelu Nicholas Asiwe Harrison Ogheneochuko Eruotor Saviour Inegbenehi Department of physiology Delta State UniversityAbraka 1Nigeria Department of physiology University of IbadanIbadan 3017Nigeria Department of physiology Adeleke UniversityEde 250Nigeria Department of pharmacology Rivers State UniversityNkpolu-Oroworukwo 5080Nigeria Department of physiology Redeemer’s UniversityEde 230Nigeria Department of Biochemistry PAMO University of Medical SciencesPort Harcourt 500211Nigeria Department of pharmacology Delta State UniversityAbraka 1Nigeria Department of Anatomy University of Port HarcourtChoba 5323Nigeria Department of Medical Laboratory Sciences University of Port HarcourtChoba 5323Nigeria

Objective:Myocardial infarction(MI)is linked to an imbalance in the supply and demand of blood oxygen in the heart muscles.Beta-blockers and calcium antagonists are just two of the common medications used to treat MI.However,these have reportedly been shown to be either ineffective or to have undesirable side effects.Extract of Ginkgo biloba leaves(GBE),a Chinese herbal product offers special compatibility benefits in therapeutic settings relating to inflammatory diseases and oxidative stress.In order to better understand how GBE affects MI in rats insulted by isoprenaline(ISO),the current study was designed.Methods:The heart weight index,serum lipid profile,cardiac marker enzymes,endogenous antioxidants[catalase(CAT),superoxide dismutase(SOD),glutathione(GSH),nitrites and malondialdehyde(MDA)],inflammatory mediators[tumour necrosis factor alpha(TNF-a)and interleukin-6(IL-6)],immunohistochemical expressions of B-cell lymphoma factor-2(Bcl-2),extracellular signal-regulated kinase(ERK1/2),and mammalian target of rapamycin(mTOR)and histopathological analysis were used to assess the cardioprotective properties of GBE.Results:The findings showed that GBE effectively attenuated myocardial infarction by boosting the body’s natural antioxidant defense system and reducing the release of inflammatory cytokines as well as heart injury marker enzymes.The expression of Bcl-2,ERK1/2 and mTOR was increased while the histomorphological alterations were reversed.Conclusion:The cardioprotective effects of GBE may be due to a mechanism involving increased Bcl-2/mTOR/ERK1/2/Na^(+),K^(+)-ATPase activity.

关键词： antioxidants extracellular signal-regulated kinase Ginkgo biloba extract isoprenaline mammalian target of rapamycin myocardial infarction Na^(+),K^(+)-ATPase

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Eubacterium coprostanoligenes alleviates chemotherapy-induced intestinal mucositis by enhancing intestinal mucus barrier

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Acta Pharmaceutica Sinica B 2024年第4期14卷 1677-1692页

作者： Dongsheng Bai Jiawei Zhao Runde Wang Jiaying Du Chen Zhou Chunyang Gu Yuxiang Wang Lulu Zhang Yue Zhao Na Lu State Key Laboratory of Natural Medicines Jiangsu Key Laboratory of Carcinogenesis and InterventionDepartment of PhysiologySchool of Basic Medicine and Clinical PharmacyChina Pharmaceutical UniversityNanjing 210009China Department of Clinical pharmacology School of PharmacyNanjing Medical UniversityNanjing 211166China

Chemotherapy-induced mucositis represents a severe adverse outcome of cancer treatment,significantly curtailing the efficacy of these treatments and,in some cases,resulting in fatal conse-quences.Despite identifying intestinal epithelial cell damage as a key factor in chemotherapy-induced mucositis,the paucity of effective treatments for such damage is evident.In our study,we discovered that Eubacterium coprostanoligenes promotes mucin secretion by goblet cells,thereby fortifying the integrity of the intestinal mucus barrier.This enhanced barrier function serves to resist microbial invasion and sub-sequently reduces the inflammatory response.Importantly,this effect remains unobtrusive to the anti-tumor efficacy of chemotherapy drugs.Mechanistically,E.copr up-regulates the expression of AUF1,leading to the stabilization of Muc2 mRNA and an increase in mucin synthesis in goblet cells.An espe-cially significant finding is that E.copr activates the AhR pathway,thereby promoting the expression of AUF1.In summary,our results strongly indicate that E.copr enhances the intestinal mucus barrier,effec-tively alleviating chemotherapy-induced intestinal mucositis by activating the AhR/AUFl pathway,consequently enhancing Muc2 mRNA stability.

关键词： Chemotherapy Mucositis Eubacterium coprostanoligenes MUC2 AUF1

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Sexual dimorphism of G protein-coupled receptor signaling in the brain

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Neural Regeneration Research 2024年第8期19卷 1635-1636页

作者： Sara Aljoudi Hamdan Hamdan Khaled S.Abd-Elrahman Department of physiology and Immunology College of Medicine and Health SciencesKhalifa UniversityAbu DhabiUnited Arab Emirates Healthcare Engineering Innovation Center(HEIC) Khalifa UniversityAbu DhabiUnited Arab Emirates Department of Anesthesiology Pharmacology and Therapeuticsand Djavad Mowafaghian Center for Brain HealthUniversity of British ColumbiaVancouverBCCanada Department of pharmacology and Therapeutics College of Medicine and Health ScienceKhalifa UniversityAbu DhabiUnited Arab Emirates Department of pharmacology and Toxicology Faculty of PharmacyAlexandria UniversityAlexandriaEgypt

G protein-coupled receptors(GPCRs)represent the most substantial family of membrane receptors that are targeted by U.S.Food and Drug Administration-approved drugs.Much of the preclinical research to understand the pharmacology of many membrane receptors including GPCRs is derived from studies in male animal models(Karp and Reavey,2019).

关键词： drugs clinical targeted

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Neuroprotective effects of resveratrol on retinal ganglion cells in glaucoma in rodents:A narrative review

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Animal Models and Experimental Medicine 2024年第3期7卷 195-207页

作者： Maryam Golmohammadi Seyed Arash Aghaei Meibodi Sulieman Ibraheem Shelash Al-Hawary Jitendra Gupta Ibrohim B.Sapaev Mazin A.A.Najm Marim Alwave Mozhgan Nazifi Mohammadreza Rahmani Mohammad Yasin Zamanian Gervason Moriasi School of Medicine Shahid Beheshti University of Medical SciencesTehranIran Department of Business Administration Business SchoolAl al-Bayt UniversityMafraqJordan Institute of Pharmaceutical Research GLA UniversityMathuraIndia Tashkent Institute of Irrigation and Agricultural Mechanization Engineers TashkentUzbekistan New Uzbekistan University TashkentUzbekistan Pharmaceutical Chemistry Department College of PharmacyAl-Ayen UniversityThi-QarIraq Medical Technical College Al-Farahidi UniversityBaghdadIraq Department of Neurology Hamadan University of Medical SciencesHamadanIran physiology-pharmacology Research Center Research Institute of Basic Medical SciencesRafsanjan University of Medical SciencesRafsanjanIran Department of physiology and pharmacology School of MedicineRafsanjan University of Medical SciencesRafsanjanIran Neurophysiology Research Center Hamadan University of Medical SciencesHamadanIran Department of pharmacology and Toxicology School of PharmacyHamadan University of Medical SciencesHamadanIran Department of Medical Biochemistry School of MedicineCollege of Health SciencesMount Kenya UniversityThikaKenya

Glaucoma,an irreversible optic neuropathy,primarily affects retinal ganglion cells(RGC)and causes vision loss and blindness.The damage to RGCs in glaucoma occurs by various mechanisms,including elevated intraocular pressure,oxidative stress,inflammation,and other neurodegenerative processes.As the disease progresses,the loss of RGCs leads to vision loss.Therefore,protecting RGCs from damage and promoting their survival are important goals in managing glaucoma.In this regard,resveratrol(RES),a polyphenolic phytoalexin,exerts antioxidant effects and slows down the evolution and progression of glaucoma.The present review shows that RES plays a protective role in RGCs in cases of ischemic injury and hypoxia as well as in ErbB2 protein expression in the retina.Additionally,RES plays protective roles in RGCs by promoting cell growth,reducing apoptosis,and decreasing oxidative stress in H_(2)O_(2)-exposed RGCs.RES was also found to inhibit oxidative stress damage in RGCs and suppress the activation of mitogen-activated protein kinase signaling pathways.RES could alleviate retinal function impairment by suppressing the hypoxia-i nducible factor-1 alpha/vascular endothelial growth factor and p38/p53 axes while stimulating the PI3K/Akt pathway.Therefore,RES might exert potential therapeutic effects for managing glaucoma by protecting RGCs from damage and promoting their survival.

关键词： glaucoma ischemic-reperfusion injury oxidative stress resveratrol retinal ganglion cells

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Fibrinogen’s potential role in connecting cerebrovascular abnormalities with glymphatic dysfunction in Alzheimer’s disease

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Neural Regeneration Research 2025年第1期20卷 203-204页

作者： Vishal Singh Arnab Choudhury Hyung Jin Ahn Department of pharmacology Physiology and NeurosciencesRutgers-New Jersey Medical SchoolNewarkNJUSA Brain Health Institute Rutgers UniversityPiscatawayNJUSA

Alzheimer’s disease(AD)stands out as the primary manifestation of age-related dementia,portraying a chronic neurodegenerative disorder distinguished by the accumulation of fibrillar amyloid-β(Aβ)plaques and neurofibrillary tangles of hyperphosphorylated tau.However,from a clinical standpoint,AD presents itself as a complex condition with a spectrum of dysfunctions rather than a singular pathological mechanism.An often-overlooked aspect of the disease is the presence of extensive cerebrovascular abnormalities,given that the majority of AD patients experience altered cerebral blood flow,damaged vasculature,increased microinfarcts and microhemorrhages.Animal models of AD further support this observation,showing cerebrovascular dysfunction such as impaired cerebral blood flow and altered cerebrovascular reactivity(Tataryn et al.,2021;Gareau et al.,2023).

关键词： cerebrovascular dysfunction Alzheimer

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Pro-resolving lipid mediator reduces amyloid-β42–induced gene expression in human monocyte–derived microglia

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Neural Regeneration Research 2025年第3期20卷 873-886页

作者： Ying Wang Xiang Zhang Henrik Biverstål Nicolas GBazan Shuai Tan Nailin Li Makiko Ohshima Marianne Schultzberg Xiaofei Li Department of Neurobiology Care Sciences&SocietyDivision of NeurogeriatricsKarolinska InstitutetStockholmSweden Department of Neurology Neuroscience CenterThe First Hospital of Jilin UniversityChangchunJilin ProvinceChina Department of physiology and pharmacology Karolinska InstitutetStockholmSweden Department of Biosciences and Nutrition Karolinska InstitutetHuddingeSweden Neuroscience Center of Excellence Louisiana State UniversityNew OrleansLAUSA Department of Medicine SolnaClinical Pharmacology GroupKarolinska University HospitalStockholmSweden

Specialized pro-resolving lipid mediators including maresin 1 mediate resolution but the levels of these are reduced in Alzheimer's disease brain, suggesting that they constitute a novel target for the treatment of Alzheimer's disease to prevent/stop inflammation and combat disease pathology. Therefore, it is important to clarify whether they counteract the expression of genes and proteins induced by amyloid-β. With this objective, we analyzed the relevance of human monocyte–derived microglia for in vitro modeling of neuroinflammation and its resolution in the context of Alzheimer's disease and investigated the pro-resolving bioactivity of maresin 1 on amyloid-β42–induced Alzheimer's disease–like inflammation. Analysis of RNA-sequencing data and secreted proteins in supernatants from the monocyte-derived microglia showed that the monocyte-derived microglia resembled Alzheimer's disease–like neuroinflammation in human brain microglia after incubation with amyloid-β42. Maresin 1 restored homeostasis by down-regulating inflammatory pathway related gene expression induced by amyloid-β42 in monocyte-derived microglia, protection of maresin 1 against the effects of amyloid-β42 is mediated by a re-balancing of inflammatory transcriptional networks in which modulation of gene transcription in the nuclear factor-kappa B pathway plays a major part. We pinpointed molecular targets that are associated with both neuroinflammation in Alzheimer's disease and therapeutic targets by maresin 1. In conclusion, monocyte-derived microglia represent a relevant in vitro microglial model for studies on Alzheimer's disease-like inflammation and drug response for individual patients. Maresin 1 ameliorates amyloid-β42–induced changes in several genes of importance in Alzheimer's disease, highlighting its potential as a therapeutic target for Alzheimer's disease.

关键词： Alzheimer's disease amyloid-β maresin microglia monocyte neuroinflammation resolution RNA-sequencing specialized pro-resolving lipid mediator

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